Prospective studies were performed of serum sickness in man. This was possible because of a NHLBI study of the treatment of aplastic anemia with horse antithymocyte globulin. Seventy per cent of treated patients developed serum sickness. In a prospective study it was shown that the onset of serum sickness in these patients could be correlated with the presence of circulating IgM containing immune complexes which bound C1q avidly. Positive RAJI assays were also noted although the amount of immune complexes noted in the latter assay was much lower than that noted by C1q binding. A new clinical finding was noted during the course of serum sickness in man and pathology of the GI system, kidney and joints was also noted in this disease. Prior to the onset of serum sickness histaminemia was noted in patients as well as an elevation in IgE levels. These studies show that in man, serum sickness follows much the same course as it does in experimental animals and validate the experimental animal model for studies of pathophysiology in man. Serologic findings associated with autoimmunity as well as clinical findings were studied in a series of 156 patients with Hereditary Angioedema. Although lupus was not a prominent finding in our patient population, a part or all of the symptom complex of Sjogren's Syndrome was a common finding in this patient group. It was noted that C1q binding activity was present in these patients. This was removable with a staph A column suggesting that IgG containing immune complexes were present in this patient group. An elevated number of helper T cells was present in the patient group as well, which was associated with decreased levels of C4 suggesting that complement activation leads to redistribution of T cells in these patients.